Search results for "down-regulation"

showing 10 items of 310 documents

Modulation of Contact Sensitivity Responses by Bacterial Superantigen

1995

Superantigens are potent modulators of the immune system, especially T cells. Therefore, we determined the influence of superantigens on the T-cell-mediated immune response, contact sensitivity. We chose the combination of staphylococcal enterotoxin B (SEB) as superantigen and 2,4-dinitrofluorbenzene (DNFB) as the contact sensitizer, because in BALB/c mice SEB reacts almost exclusively with V beta 8+ T cells, and these cells are capable of transferring contact sensitivity to DNFB from sensitized donors to naive syngeneic recipients. Pretreatment with a single intradermal injection of 50 ng SEB 24 h before DNFB exposure at the same site on the lower abdomen enhanced the induction of contact …

Lymphoid Tissue24-dinitrofluorbenzeneReceptors Antigen T-Cell alpha-betaT-LymphocytesDown-Regulationchemical and pharmacologic phenomenaDermatologyEnterotoxinDermatitis Contactcontact sensitivityBacterial superantigenBiochemistrysuperantigenProinflammatory cytokineEnterotoxinsInterferon-gammaMiceImmune systemmedicineSuperantigenAnimalsIntradermal injectionMolecular BiologySensitizationSkinAntigens BacterialMice Inbred BALB CSuperantigensbusiness.industryhemic and immune systemsCell BiologyContact sensitivitybiological factorsStaphylococcal enterotoxin Bmedicine.anatomical_structureImmunologyDinitrofluorobenzeneFemaleImmunizationbusinessJournal of Investigative Dermatology
researchProduct

HSPH1 inhibition downregulates Bcl-6 and c-Myc and hampers the growth of human aggressive B-cell non-Hodgkin lymphoma

2015

We have shown that human B-cell non-Hodgkin lymphomas (B-NHLs) express heat shock protein (HSP)H1/105 in function of their aggressiveness. Here, we now clarify its role as a functional B-NHL target by testing the hypothesis that it promotes the stabilization of key lymphoma oncoproteins. HSPH1 silencing in 4 models of aggressive B-NHLs was paralleled by Bcl-6 and c-Myc downregulation. In vitro and in vivo analysis of HSPH1-silenced Namalwa cells showed that this effect was associated with a significant growth delay and the loss of tumorigenicity when 10(4) cells were injected into mice. Interestingly, we found that HSPH1 physically interacts with c-Myc and Bcl-6 in both Namalwa cells and pr…

Lymphoma B-CellXenograft Model Antitumor AssayDNA-Binding ProteinImmunologyDown-RegulationMice SCIDSettore MED/08 - Anatomia PatologicaBiologyBiochemistryHSP110 Heat-Shock ProteinProto-Oncogene Proteins c-mycMiceDownregulation and upregulationimmune system diseasesCell Line Tumorhemic and lymphatic diseasesHeat shock proteinGene Knockdown TechniquesmedicineAnimalsHumansGene silencingHSP110 Heat-Shock ProteinsAnimals; Cell Line Tumor; DNA-Binding Proteins; Down-Regulation; Gene Knockdown Techniques; HSP110 Heat-Shock Proteins; Humans; Lymphoma B-Cell; Mice; Mice SCID; Proto-Oncogene Proteins c-myc; Xenograft Model Antitumor Assays; Biochemistry; Immunology; Medicine (all); Hematology; Cell BiologyAnimalMedicine (all)Cell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysIn vitroLymphomaDNA-Binding ProteinsCell cultureGene Knockdown TechniquesGene Knockdown TechniqueImmunologyProto-Oncogene Proteins c-bcl-6Cancer researchB-Cell Non-Hodgkin LymphomaHumanBlood
researchProduct

Regulation of ERK1/2 activity upon contact inhibition in fibroblasts.

2011

Contact inhibition is a crucial mechanism regulating proliferation in vitro and in vivo. Despite its generally accepted importance for maintaining tissue homeostasis knowledge about the underlying molecular mechanisms of contact inhibition is still scarce. Since the MAPK ERK1/2 plays a pivotal role in the control of proliferation, we investigated regulation of ERK1/2 phosphorylation which is downregulated in confluent NIH3T3 cultures. We found a decrease in upstream signaling including phosphorylation of the growth factor receptor adaptor protein ShcA and the MAPK kinase MEK1/2 in confluent compared to exponentially growing cultures whereas involvement of ERK1/2 phosphatases in ERK1/2 inact…

MAPK/ERK pathwayCell signalingBiophysicsDown-RegulationCell CommunicationBiochemistryReceptor Platelet-Derived Growth Factor betaMiceGrowth factor receptorAnimalsReceptors Platelet-Derived Growth FactorPhosphorylationMolecular BiologyTissue homeostasisCell ProliferationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologySignal transducing adaptor proteinContact inhibitionCell BiologyFibroblastsMolecular biologyCell biologyErbB Receptorsbiology.proteinNIH 3T3 CellsPhosphorylationPlatelet-derived growth factor receptorBiochemical and biophysical research communications
researchProduct

Involvement of the transcription factor FoxM1 in contact inhibition

2012

Contact inhibition is a crucial mechanism regulating proliferation in vitro and in vivo. Although it is generally accepted that contact inhibition plays a pivotal role in maintaining tissue homeostasis, the molecular mechanisms of contact inhibition are still not fully understood. FoxM1 is known as a proliferation-associated transcription factor and is upregulated in many cancer types. Vice versa, anti-proliferative signals, such as TGF-β and differentiation signals decrease FoxM1 expression. Here we investigated the role of FoxM1 in contact inhibition in fibroblasts. We show that protein expression of FoxM1 is severely and rapidly downregulated upon contact inhibition, probably by inhibiti…

MAPK/ERK pathwayCyclin ABiophysicsDown-RegulationCell Cycle ProteinsCyclin AProtein Serine-Threonine KinasesBiochemistryMiceDownregulation and upregulationProto-Oncogene ProteinsAnimalsPhosphorylationRNA Small InterferingExtracellular Signal-Regulated MAP KinasesMolecular BiologyTranscription factorTissue homeostasisbiologyContact InhibitionKinaseForkhead Box Protein M1Contact inhibitionForkhead Transcription FactorsCell BiologyG1 Phase Cell Cycle CheckpointsCell biologyNIH 3T3 Cellsbiology.proteinEctopic expressionBiochemical and Biophysical Research Communications
researchProduct

Induction of collagenase-3 (MMP-13) expression in human skin fibroblasts by three-dimensional collagen is mediated by p38 mitogen-activated protein k…

1999

Collagenase-3 (matrix metalloproteinase-13, MMP-13) is a recently identified human MMP with an exceptionally wide substrate specificity and restricted tissue-specific expression. Here we show that MMP-13 expression is induced in normal human skin fibroblasts cultured within three-dimensional collagen gel resulting in production and proteolytic activation of MMP-13. Induction of MMP-13 mRNAs by collagen gel was potently inhibited by blocking antibodies against alpha1 and alpha2 integrin subunits and augmented by activating antibody against beta1 integrin subunit, indicating that both alpha1 beta1 and alpha2 beta1 integrins mediate the MMP-13-inducing cellular signal generated by three-dimens…

MAPK/ERK pathwayIntegrinsReceptors CollagenSB 203580IntegrinDown-RegulationBiologyBiochemistryp38 Mitogen-Activated Protein KinasesCollagen receptorIntegrin alpha1beta1chemistry.chemical_compoundTransforming Growth Factor betaMatrix Metalloproteinase 13medicineHumansCollagenasesProtein kinase AMolecular BiologyDNA PrimersSkinBase SequenceKinaseTumor Necrosis Factor-alphaCell BiologyFibroblastsProtein-Tyrosine KinasesMolecular biologyEnzyme ActivationchemistryCalcium-Calmodulin-Dependent Protein KinasesCollagenasebiology.proteinCollagenMitogen-Activated Protein KinasesTyrosine kinasemedicine.drugInterleukin-1The Journal of biological chemistry
researchProduct

The Late Endosomal Adaptor Molecule p14 (LAMTOR2) Regulates TGFβ1-Mediated Homeostasis of Langerhans Cells

2014

Langerhans cells (LCs), a sub-population of dendritic cells (DCs) in the skin, participate in the regulation of immunity and peripheral tolerance. The adaptor molecule p14 is part of the late endosomal/lysosomal adaptor and mitogen-activated protein kinase and mammalian target of rapamycin (mTOR) activator/regulator (LAMTOR) complex, which mediates the activation of lysosome-associated extracellular signaling regulated kinase (ERK) and the mTOR cascade. In previous work, we demonstrated that CD11c-specific deficiency of p14 disrupts LC homeostasis by affecting the LAMTOR-mediated ERK and mTOR signaling. In this study, we extended our analysis on p14 deficiency specifically in LCs. Langerin-…

MAPK/ERK pathwayMaleMAP Kinase Signaling SystemReceptor Transforming Growth Factor-beta Type IDown-Regulationchemical and pharmacologic phenomenaEndosomesDermatologyBiologyProtein Serine-Threonine KinasesDermatitis ContactBiochemistryArticleImmune toleranceImmunophenotypingTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementImmune ToleranceAnimalsHomeostasisProtein kinase AMolecular BiologyPI3K/AKT/mTOR pathway030304 developmental biologySkin0303 health sciencesintegumentary systemKinaseReceptor Transforming Growth Factor-beta Type IIPeripheral toleranceProteinshemic and immune systemsCell BiologyMice Mutant StrainsCell biologyCD11c AntigenLangerhans CellsFemaleReceptors Transforming Growth Factor beta030215 immunologyTransforming growth factorJournal of Investigative Dermatology
researchProduct

Down-regulation of human CYP3A4 by the inflammatory signal interleukin-6: molecular mechanism and transcription factors involved.

2002

The hepatic drug-metabolizing cytochrome P-450 (CYP) enzymes are down-regulated during inflammation. In vitro studies with hepatocytes have shown that the cytokines released during inflammatory responses are largely responsible for this CYP repression. However, the signaling pathways and the cytokine-activated factors involved remain to be properly identified. Our research has focused on the negative regulation of CYP3A4 (the major drug-metabolizing human CYP) by interleukin 6 (IL-6) (the principal regulator of the hepatic acute-phase response). CYP3A4 down-regulation by IL-6 requires activation of the glycoprotein receptor gp130; however, it does not proceed through the JAK/STAT pathway, a…

MAPK/ERK pathwaySTAT3 Transcription FactorMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesDown-RegulationBiologyBiochemistryTransactivationCytochrome P-450 Enzyme SystemAntigens CDGeneticsCCAAT-Enhancer-Binding Protein-alphaCytokine Receptor gp130Tumor Cells CulturedCytochrome P-450 CYP3AHumansRNA MessengerSTAT3Molecular BiologyTranscription factorCells CulturedMembrane GlycoproteinsDose-Response Relationship DrugInterleukin-6Reverse Transcriptase Polymerase Chain ReactionCCAAT-Enhancer-Binding Protein-betaJAK-STAT signaling pathwayProtein-Tyrosine KinasesGlycoprotein 130Molecular biologyDNA-Binding ProteinsGene Expression Regulationbiology.proteinHepatocytesTrans-ActivatorsSignal transductionBiotechnologyAcute-Phase ProteinsSignal TransductionTranscription FactorsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
researchProduct

A role for miR-142-3p in colony-stimulating factor 1-induced monocyte differentiation into macrophages

2013

AbstractThe differentiation of human peripheral blood monocytes into macrophages can be reproduced ex vivo by culturing the cells in the presence of colony-stimulating factor 1 (CSF1). Using microarray profiling to explore the role of microRNAs (miRNAs), we identified a dramatic decrease in the expression of the hematopoietic specific miR-142-3p. Up- and down-regulation of this miRNA in primary human monocytes altered CSF1-induced differentiation of monocytes, as demonstrated by changes in the expression of the cell surface markers CD16 and CD163. One of the genes whose expression is repressed by miR-142-3p encodes the transcription factor Early Growth Response 2 (Egr2). In turn, Egr2 assoc…

Macrophage colony-stimulating factorAntigens Differentiation MyelomonocyticDown-RegulationChronic myelomonocytic leukemiaReceptors Cell SurfaceCD16BiologyGPI-Linked ProteinsMonocyte–macrophage differentiationMonocytesChronic myelomonocytic leukemiaAntigens CDCell Line TumorMiR-142-3pmedicineHumansTranscription factorMolecular BiologyEarly Growth Response Protein 2Early Growth Response Protein 1Cluster of differentiationMolecular circuitryMacrophage Colony-Stimulating FactorMacrophagesReceptors IgGCell DifferentiationLeukemia Myelomonocytic ChronicCell Biologymedicine.diseaseUp-RegulationRepressor ProteinsMicroRNAsHaematopoiesisMonocyte differentiationCancer researchEgr2K562 CellsK562 cellsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
researchProduct

Suppressing an Anti-Inflammatory Cytokine Reveals a Strong Age-Dependent Survival Cost in Mice

2010

7 pages; International audience; BACKGROUND: The central paradigm of ecological immunology postulates that selection acts on immunity as to minimize its cost/benefit ratio. Costs of immunity may arise because the energetic requirements of the immune response divert resources that are no longer available for other vital functions. In addition to these resource-based costs, mis-directed or over-reacting immune responses can be particularly harmful for the host. In spite of the potential importance of immunopathology, most studies dealing with the evolution of the immune response have neglected such non resource-based costs. To keep the immune response under control, hosts have evolved regulat…

Male0106 biological sciencesSurvivalmedicine.medical_treatmentAnti-Inflammatory AgentsImmunology/ImmunomodulationDown-Regulationlcsh:MedicineInflammationBiology[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology010603 evolutionary biology01 natural sciencesAntibodiesMice03 medical and health sciencesImmune systemImmunityImmunopathologymedicineAnimalsReceptors Interleukin-10lcsh:ScienceReceptor030304 developmental biologyInflammationEvolutionary Biology[ SDE.BE ] Environmental Sciences/Biodiversity and Ecology0303 health sciencesMultidisciplinarylcsh:RAge FactorsInterleukin-103. Good healthMice Inbred C57BLInterleukin 10CytokineEcology/Physiological Ecology[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyImmunologybiology.proteinlcsh:Q[SDE.BE]Environmental Sciences/Biodiversity and Ecologymedicine.symptomAntibodyResearch ArticlePLoS ONE
researchProduct

Identification of periplakin as a major regulator of lung injury and repair in mice

2018

IF 12.784 (2016); International audience; Periplakin is a component of the desmosomes that acts as a cytolinker between intermediate filament scaffolding and the desmosomal plaque. Periplakin is strongly expressed by epithelial cells in the lung and is a target antigen for autoimmunity in idiopathic pulmonary fibrosis. The aim of this study was to determine the role of periplakin during lung injury and remodeling in a mouse model of lung fibrosis induced by bleomycin. We found that periplakin expression was downregulated in the whole lung and in alveolar epithelial cells following bleomycin-induced injury. Deletion of the Ppl gene in mice improved survival and reduced lung fibrosis developm…

Male0301 basic medicinePulmonologylcsh:MedicineMouse modelsMiceIdiopathic pulmonary fibrosischemistry.chemical_compoundFibrosisPeriplakinMice KnockoutLung InjuryGeneral Medicinerespiratory system3. Good healthmedicine.anatomical_structureCytokinesmedicine.symptomSignal TransductionResearch ArticleCell signalingDown-RegulationInflammationRespiratory MucosaLung injuryBleomycinBleomycin03 medical and health sciencesmedicineAnimalsHumansInflammationLung030102 biochemistry & molecular biologybusiness.industryMacrophagesPlakinslcsh:Rmedicine.diseaseFibrosisIdiopathic Pulmonary Fibrosisrespiratory tract diseasesMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryAlveolar Epithelial CellsCancer researchbusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyJCI Insight
researchProduct